Colorectal cancer is a digestive tract malignancy and the third leading cause of cancer?related mortality worldwide. Norcantharidin (NCTD), the demethylated form of cantharidin, has been reported to possess anticancer properties. Family?with?sequence?similarity?46c (Fam46c), a non?canonical poly(A) polymerase, has been reported to be critical in NCTD?mediated effects in numerous types of cancer, including hepatoma. In the current study, it was found that Fam46c expression was reduced in colorectal cancer tissues and cells. Treatment with NCTD was observed to significantly enhance apoptosis and inhibit glycolysis in colorectal cancer cells. In addition, Fam46c and cleaved caspase 3 expression levels were found to be increased in response to NCTD treatment, in contrast to tumor?specific pyruvate kinase M2 and phosphorylated ERK expression, which was reduced. Importantly, overexpression of Fam46c exerted similar effects as NCTD treatment on the apoptosis and glycolysis of colorectal cancer cells, whereas Fam46c knockdown strongly attenuated the effect of NCTD. Moreover, epidermal growth factor, which acts as an agonist of ERK1/2 signaling, weakened the effects of NCTD on colorectal cancer cells. Taken together, the results indicated that NCTD promotes apoptosis and suppresses glycolysis in colorectal cancer cells by possibly targeting Fam46c and inhibiting ERK1/2 signaling, hence suggesting that Fam46c may act as a tumor suppressor in colorectal cancer. Thus, the present study identified a novel therapeutic target of NCTD in the clinical treatment of colorectal cancer.Following the publication of the above article, the authors noted that an incorrect version of Fig. 8 had been included. Essentially, the data presented as panel (B) in this figure should not have been included; there is only one data panel in this figure. The corrected version of Fig. 8 is shown opposite. https://www.selleckchem.com/products/deferoxamine-mesylate.html Secondly, the authors have realized that, in the main title and in the running title, exendin?4 was incorrectly spelt as "extendin?4". The correct version of the title, as it should have appeared in this paper, is shown above. Note that these errors do not alter the interpretation of the results and conclusions, and all the authors agree to this corrigendum. The authors apologize to the readership of the Journal for any confusion these errors have caused. [the original article was published in Molecular Medicine Reports 12 3007-3016, 2015; DOI 10.3892/mmr.2015.3682].Advanced glycosylation end-product specific receptor (AGER) is a multi-ligand cell surface receptor abnormally expressed in lung cancer, and is a member of the immunoglobulin superfamily. Therefore, this study aimed to explore the effect of AGER on the biological behavior of non?small cell lung cancer (NSCLC) H1299 cell line. A microarray?based gene expression profiling analysis of the GSE27262 dataset from the Gene Expression Omnibus (GEO) database was conducted to identify differentially expressed genes, which were verified using The Cancer Genome Atlas (TCGA) database. The expression of AGER in the normal human lung BEAS?2B cell line and NSCLC H1299 cell line was examined using reverse transcription?quantitative PCR. Lentiviral interference and overexpression vectors of AGER were constructed and transfected into H1299 cells using Lipofectamine®. AGER expression and biological properties, including cell viability, apoptosis, migration and invasion abilities, in H1299 cells were investigated using MTT, flow cytometry, wound healing and Transwell assays. AGER was expressed at a low level in NSCLC tissues and H1299 cells (P less then 0.05). Compared with control cells, AGER overexpression cells displayed decreased cell viability, proliferation, migration and invasion abilities, and significantly increased levels of apoptosis. Furthermore, AGER overexpression increased the expression of Bax and decreased the expression of Bcl?2 in H1299 cells (P less then 0.05), and AGER knockdown displayed the opposite effects on H1299 cells. Therefore, AGER overexpression decreased the proliferation, invasion and migration abilities of H1299 cells, and increased apoptosis. The present study suggested that AGER might serve as a potential molecular marker for NSCLC.Neural stem/progenitor cells (NSPCs) remain in the mammalian brain throughout life, where they have the ability to self?renew and generate different types of cell in the central nervous system (CNS). Therefore, NSPCs may be a potential novel therapeutic strategy following damage to the CNS. Previous research has reported that microRNA (miR)?29a served an important role in regulating cell proliferation, differentiation and survival; however, to the best of our knowledge, little is known of the effect of miR?29a in neural differentiation. The present study aimed to investigate the effect of miR?29a on the differentiation of NSPCs, determined via RNA interference, immunostaining, reverse transcription-quantitative PCR and western blotting. The present study discovered that the expression levels of miR?29a were significantly upregulated in a 02:54:50dependent manner during neural differentiation. Immunostaining showed that overexpression of miR?29a promoted neural differentiation, which manifested in increased expression levels of neuron?specific class III β?tubulin (Tuj1); however, miR?29a had no effect on neuroglial differentiation. The expression levels of Kruppel?like factor 4 (KLF4) were downregulated following overexpression of miR?29a, whereas the inhibition of miR?29a demonstrated the opposite effect. These results suggested that the overexpression of miR?29a may promote neural differentiation in cultured rat NSPCs by decreasing the expression levels of KLF4. Thus indicating that targeting KLF4, a crucial regulatory factor for the maintenance of stemness, may be a potential underlying mechanism of action for miR?29a. In conclusion, the findings of the present study identified a potential mechanism of action for miR?29a in NSPC differentiation and provided a novel insight into the treatment strategies for CNS damage.